Asbestos exposure in New Zealand:

Transcription

1 Asbestos exposure in New Zealand: Review of the scientific evidence of non-occupational risks A report on behalf of the Royal Society of New Zealand and the Office of the Prime Minister s Chief Science Advisor April 2015

3 8 April 2015 Hon Dr Jonathan Coleman Minister of Health Dear Dr Coleman, The following report is provided in response to a request by the Ministry of Health in late 2014 to the Prime Minister s Chief Science Advisor (PMCSA) and the Royal Society of New Zealand (RSNZ) to review the available scientific evidence about health risks of casual exposure to asbestos in the non- occupational environment. The Prime Minister approved the engagement of the PMCSA. We were asked specifically to analyse data pertaining to risks from asbestos exposure to residents of older houses undergoing renovation and repair work, such as that which has been carried out and is ongoing in the aftermath of the Canterbury earthquakes. The complexity, urgency and scale of the rebuild in Canterbury resulted in some remediation activities involving asbestos being undertaken without full compliance with recommended safety procedures, and this has caused considerable concern among the public. The aim was to provide government decision makers with a comprehensive and up- to- date understanding of the possible levels of exposure encountered during these activities and their potential risks to health, so that reliable risk communication messages could be conveyed to the general public, and to assist further consideration of how to reduce future risks where they might be encountered. Process This scientific review was conducted in accord with a general process agreed between the Office of the PMCSA and the President of the RSNZ for such reports. The PMSCA appointed an experienced research analyst to undertake the primary research and literature reviews. Following an initial scoping that included an extensive reading of the literature (informal, grey and peer reviewed) on the subject, a draft table of contents was agreed between the PMCSA and the President of the RSNZ. The RSNZ then appointed a panel of appropriate experts across the relevant disciplines that was approved by the PMCSA. A member of civil society with long experience in Canterbury issues, Hon Margaret Austin, CNZM, was invited to be an observer to the panel and to be included in the discussions and drafting to be sure that it met local community concerns and needs. The research analyst in the Office of the PMCSA produced an early partial draft of the report that was presented to a meeting of the expert panel, and the input of panel members was sought both as to framing of the report and interpretation of the literature. Over the following weeks, the panel members joined in an iterative process with the research analyst to develop the report. In its advanced form all the members of the panel, together with the PMCSA and the President of the RSNZ, agreed via exchange on the wording of the report and its executive summary. In this form it was sent out for international peer review by scientific experts in Australia and the UK. Representatives from the Ministry of Health were also provided with an opportunity to comment on the draft. Following receipt and consideration of all comments, the report and executive summary were returned to the panel for final review and approval. iii

4 Findings and recommendations Like most developed countries, New Zealand has a legacy of asbestos use primarily in the construction industry that spans many decades. Despite cessation of the production and most uses of asbestos- containing materials (ACMs) in this country in the 1980s, the hazard remains in many buildings and homes that were constructed during the periods of heavy asbestos use. While no ACMs are manufactured in New Zealand, there may still be some importation, as this is not rigorously controlled. There are regulations covering exposure of workers to asbestos. The evidence suggests that if bonded (non- friable) ACMs are maintained in good condition, they do not pose a health risk to building occupants. However, uncontrolled removal or repair of such materials, or their extensive deterioration may cause release of asbestos fibres, which are known to be hazardous if inhaled. The amount of asbestos released during work such as removal of sprayed- on asbestos coatings or during sanding of asbestos backing after lifting tile or vinyl flooring can be significant if proper procedures are not followed, but does not typically exceed workplace regulatory levels. Exposure levels associated with most home renovation activities are generally orders of magnitude lower than historical occupational exposures that are known to increase the risk of asbestos- related diseases. The main potential outcome of concern related to such low exposures is mesothelioma, which is associated with much lower cumulative exposures to asbestos fibres than lung cancer or other asbestos- related lung diseases and cancers. Most asbestos- containing materials used in New Zealand houses contain mainly chrysotile asbestos, which confers a lower risk of mesothelioma than other asbestos types. While there is no absolutely safe level of asbestos exposure, asbestos fibres in very low concentrations also exist in the natural environment, and therefore some exposure is unavoidable. The risk at very low exposure levels needs to be in put in the context of other inevitable risks, such as low- level radiation exposure during an aeroplane flight, for which no minimal safe dose is known. The report concludes that remediation activities such as those that have taken place in Canterbury are unlikely to result in any significant increase in risk to homeowners and occupants of damaged houses, unless they were performing the work themselves, without taking proper precautions such as wetting the surfaces and using a respirator. Although these conclusions should be reassuring for many home- owners, they do not provide grounds for complacency Our about the risks for people working with asbestos - including residents doing their own Our assessment assessment suggests suggests that that it is it appropriate, is appropriate, from from the the scientific scientific perspective, perspective, that that renovations. Messages about the importance of consistently taking adequate precautions when working with fluoridation be expanded to assist those New Zealand communities that currently do ACMs fluoridation should be reinforced. be expanded to assist those New Zealand communities that currently do not not benefit benefit from from this this public public health health measure measure particularly particularly those those with with a high a high prevalence prevalence of dental of dental caries. caries. The report also notes that many countries have now banned the importation and continued use of ACMs and recommends that New Zealand should similarly consider introducing such a ban. Yours Yours sincerely sincerely Yours sincerely Sir Peter Gluckman Prime Minister s Chief Science Advisor Sir Peter Sir Peter Gluckman Gluckman Prime Prime Minister s Minister s Chief Chief Science Science Advisor Advisor Sir David Skegg President, Royal Society of New Zealand Sir David Sir David Skegg Skegg President, President, Royal Royal Society Society of New of New Zealand Zealand iv

5 Acknowledgements This report was commissioned by Sir Peter Gluckman, the New Zealand Prime Minister s Chief Science Advisor (PMCSA), and Sir David Skegg, the President of the Royal Society of New Zealand (RSNZ), at the request of the New Zealand Ministry of Health. The report was prepared by Dr. Anne Bardsley, PhD, Research Analyst in the PMCSA office, working in collaboration with an Expert Panel appointed by the RSNZ. The report was peer reviewed by three international experts before its release. Advisors from the New Zealand Ministry of Health provided comments on an interim draft. Expert Panel Members Michael Beasley, MBChB, MSc, DComH, DIH, FFOM, Medical Toxicologist, National Poisons Centre, Preventive & Social Medicine, University of Otago, Dunedin, New Zealand Cheryl Brunton, MBChB, DComH, FNZCPHM, Senior Lecturer, Department of Population Health, University of Otago; and Public Health Specialist and Medical Officer of Health, Community and Public Health, Canterbury District Health Board, Christchurch, New Zealand David Johnston, MSc, PhD, MInstD, Director/Professor, Joint Centre for Disaster Research, GNS Science/Massey University, Wellington, New Zealand Diana Sarfati, MBChB, MPH, PhD, FNZCPHM, Associate Professor, Department of Public Health, University of Otago, Wellington, New Zealand Panel Lay Observer Hon Margaret Austin, CNZM, Former Vice President, Science Education, Royal Society of New Zealand, Christchurch, New Zealand International reviewers Bruce Armstrong, AM, FAA, BMedSc, MBBS, DPhil, FRACP, FAFPHM, Emeritus Professor, School of Public Health, The University of Sydney; Senior Adviser, The Sax Institute; and Chairman, Bureau of Health Information, Sydney, Australia Tim Driscoll, BSc, MBBS, MOHS, PhD, Professor of Epidemiology and Occupational Medicine, University of Sydney, Sydney, Australia Julian Peto, MA, DSc, FMedSci, Professor of Epidemiology, London School of Hygiene & Tropical Medicine, London, UK v

7 Asbestos exposure in New Zealand: Review of the scientific evidence of nonoccupational risks The purpose of this report is to provide a comprehensive and up-to-date understanding of the scientific evidence on the risks from casual asbestos exposure in the non-occupational environment in New Zealand, specifically addressing the level of risk to occupants of houses containing asbestos, and of exposure during renovations and repairs. The potential effects of events such as the Canterbury earthquakes and consequent rebuild on exposures and risk are considered. The intent of this report is to inform decision-making on asbestos management and consequent public health measures including risk communication to the public. In order to assess asbestos risks in the residential environment, it was necessary to use the evidence base established by investigations in historical occupational settings, where asbestos exposure was very much higher and the association of such exposure with adverse outcomes was clear. Although the report discusses exposures that may be encountered by workers today who are involved in building construction, renovation, remediation and demolition, we caution readers not to treat the analysis of occupational risks as definitive; the information is provided to assist with understanding the non-occupational risks. Executive Summary Asbestos is a term referring to a group of related, naturally-occurring fibrous silicate minerals that have been mined extensively around the world and were once widely used industrially and in building construction because of their characteristic strength, pliability, insulating properties, and resistance to fire and chemical breakdown. Over time, asbestos was linked to a number of serious lung diseases and cancers in workers who were heavily exposed to its raw fibres in mines, mills, and factories producing asbestos products. Asbestos-related diseases were later observed in workers who regularly handled these products, and in people environmentally exposed to airborne fibre contamination near asbestos mines and factories. Inhalation exposure to asbestos is now known to be a serious public health risk, with consequential disease liable to develop after a long latency period the risk of which is influenced by the intensity (dose), the frequency, and the duration of the exposure (i.e. the cumulative amount breathed in). Although other routes of exposure are possible (e.g. dermal contact, ingestion), inhalation is the only route that has been established as causing harm. Fibrotic lung diseases (pleural changes and asbestosis), lung cancer, malignant mesothelioma, laryngeal cancer, ovarian cancer and possibly other cancers can occur 20 to 50 years after heavy exposure to asbestos fibres. The risk of developing disease from asbestos inhalation increases with increasing cumulative exposure. Efforts to reduce and ultimately to eliminate this risk have led to total prohibition of the production, importation and use of asbestos in many countries, and strict regulation of exposure of workers involved in repairing or removing asbestos-containing materials (ACMs). The presence of ACMs throughout many older homes and buildings means that the asbestos hazard still lingers, and non- 1

8 occupational exposure of the public is an ongoing risk, although the magnitude of this risk is not well characterized. This report aims to summarise the available evidence in order to inform policymakers and the public about the extent of risk from non-occupational exposure to ACMs in residential houses in New Zealand, and potential actions to be taken. Asbestos exposure in New Zealand Unprocessed asbestos was imported into New Zealand beginning in the late 1930s and building products composed of asbestos mixed with cement were produced over a 50-year period up until the mid-1980s. ACMs used in building construction were also imported from other countries. Many of these products were used in the construction of New Zealand houses between 1940 and The incidence of asbestos-related diseases has been rising in New Zealand in accord with the expected latency from past heavy exposure of workers in the asbestos industry, and those working regularly with ACMs (e.g. construction workers). Although New Zealand lagged behind many other countries in dealing with the asbestos hazard, regulations on its use and on acceptable workplace exposure levels have ended the era of very high occupational exposure risk, and a decline in asbestos-related disease incidence is to be expected in the future. However the legacy of past asbestos use in New Zealand persists in the numerous ACMs that remain in place in older buildings and houses, including asbestos cement roofing, external cladding, internal wall linings, textured ceilings, vinyl flooring, and insulation around pipes and hot water heaters. The necessity of large numbers of building and infrastructure demolitions as a result of the Canterbury earthquakes of 2010 and 2011 has increased awareness of asbestos, and the possibility of exposure to asbestos from ACMs in damaged older homes. There has been public concern that improper handling of asbestos in homes undergoing renovation and repair during the Canterbury rebuild may have exposed people to dangerous levels of airborne asbestos fibres. The main concern is exposure of the public to friable asbestos that which is loosely bonded and can be crumbled or reduced to powder by hand pressure. Asbestos is considered non-friable if it is bonded within building materials and is therefore more resistant to mild abrasion or damage. Non-friable ACMs that are in good condition do not release fibres and do not pose a health risk, but they can become friable when damaged or weathered, or during remediation, repair or removal. Risk characterization and assessment Asbestos has been clearly shown to be a hazardous material with the propensity to cause cancer and other diseases in exposed individuals. The risks associated with asbestos depend on the extent and intensity of the exposure to the hazard and the possible underlying risk factors or susceptibilities of the individual. Risks also differ depending on the type of asbestos to which an individual is exposed. Asbestos fibres are naturally ubiquitous at very low levels in air and water, and therefore there are no completely unexposed populations. Nonetheless, there is no level of exposure that is known to carry no risk of asbestos-related disease. Asbestos types and potency All asbestos types can cause asbestos-related cancers. However, the different chemical composition and structures of the asbestos types affect their toxicity and persistence in lung and pleural tissues resulting in differences in carcinogenic potential. There are three common asbestos types that have been used industrially. Amosite and crocidolite are of the amphibole variety - they have straight fibre structures and are highly insoluble in lung fluid, and thus can persist in lung tissues for decades after inhalation. The third, and by far the most commonly used type in New Zealand, is chrysotile, which has a curly fibre structure and is relatively more soluble and more readily cleared from the lungs than the amphiboles. Estimates from different studies vary, but it is generally acknowledged that the cancer risk is higher from amphibole exposure than from chrysotile exposure. One estimate of the 2

9 ratio of the potency for inducing mesothelioma suggested that chrysotile is up to 500x less potent than crocidolite, and 100x less potent than amosite. Nonetheless, all forms of asbestos are considered to be carcinogenic, and therefore hazardous. Dose, duration, and cumulative exposure Epidemiological studies suggest that the level of risk of asbestos-induced cancer is directly related to the cumulative asbestos exposure received (the amount breathed in) over a period of time. This means that a small number of high-exposure incidents may confer roughly the same risk as a larger number of lower-exposure incidents. However, because of the long latency between accumulated exposure and cancer development, a given cumulative exposure accrued over a short period is expected to result in a higher risk of actually developing a cancer than the same exposure accrued over a longer period, if both exposures were to begin at the same time. This is because a substantial portion of the longer exposure will occur at older ages, when the potential to experience the full latency period is less likely. Exposure level estimation Asbestos is found in certain types of rock formations, and is present at very low levels in air and water as a result of natural erosion processes. However, industrial activities have greatly increased the levels of airborne asbestos fibres in some locations and situations. Environmental exposure has been high in the vicinity of working asbestos mines and factories. Levels are elevated around motorways and in cities, because of release of asbestos fibres from many automotive brake linings. The large amount of existing asbestos cement products making up the exterior cladding and roofs of many buildings and homes also contributes to a significant release of asbestos fibres into the total environment each year. This report is primarily concerned with the airborne asbestos levels that may be found within homes where friable ACMs are present, and human exposures during repair or removal of such materials when the work has been carried out by others. The potential risk to building occupants posed by the presence of old ACMs has been the subject of intense debate, but studies suggest that undisturbed ACMs do not cause elevated airborne asbestos concentrations inside buildings. Fibre release episodes from small repair or maintenance activities or from random dislodging of ACMs also do not substantially increase average concentrations inside buildings, although they might result in exposure to an individual undertaking such work or present nearby. Risks of low-level exposure While the risk associated with working with raw asbestos or regularly handling ACMs as part of an occupation is relatively well understood, the level of risk arising from occasional, low exposures is more difficult to assess. The vast majority of data relating asbestos exposure to disease risk have come from studies of heavily-exposed groups in asbestos mining, milling, transport and manufacturing industries, or other occupational groups working with asbestos products (e.g. construction trades, ship builders, mechanics, etc.). Assessment of risks of low-level asbestos exposure has had to rely on extrapolation from studies of such highly-exposed workers in order to estimate risk for disease development in minimally-exposed non-occupational groups. A degree of uncertainty in assessing these risk levels is unavoidable, as knowledge of dose-response relationships at low exposure is limited by methodological and technical considerations. In particular, the incidence of lung cancer attributable to asbestos exposure is difficult to quantify, because there is a substantial background incidence due to factors other than exposure to asbestos (mainly tobacco smoking). Whereas a substantially elevated incidence of lung cancer can be quantified in highly-exposed worker populations, any increase above background rates resulting from low-level, non-occupational asbestos exposure would be difficult to detect, and has not been 3

10 reported (though the risk should not be considered as nil). Current non-occupational exposure levels are also considered to be too low to cause asbestosis. Mesothelioma, which is a highly specific outcome of asbestos exposure, occurs at lower exposure levels than asbestosis or lung cancer and is the disease most likely to occur in relation to non-occupational exposures. This report thus focuses mainly on the risk of mesothelioma, as the low exposures to the general public of New Zealand today are not likely to increase the risk of any other asbestos-related diseases. Reports of mesothelioma resulting from exposure to asbestos in the non-occupational setting have been increasing in many countries, although most involve environmental exposures related to residence near asbestos mines or factories. Exposure estimates have not been reported in such populations, so it is difficult to relate these risks to other non-occupational exposures, such as those encountered by occupants of houses with damaged or deteriorating ACMs or who have undertaken or been present during ACM repair or removal. The health risk to most building occupants appears to be very low. There is no evidence that a single peak in exposure of the kind encountered during maintenance or repair of ACMs significantly affects disease risk, although each incident of such exposure would add to an individual s cumulative exposure. Risk assessment in the Canterbury Home Repair Programme Earthquake damage to ACMs, as well as the removal and repair processes could cause release of asbestos fibres from previously non-friable materials, potentially resulting in elevated exposure and health risks. The use of proper abatement and cleanup procedures can effectively reduce these increased risks. For example, most asbestos removal procedures involve wetting the surface to reduce the release of dust. Dry scraping or sanding of friable ACMs should be avoided. In the immediate aftermath of the Canterbury earthquakes, cleanup procedures and home remediation did not always follow appropriate guidelines for avoiding asbestos exposure. The level of exposure to workers and the public during this time is not known with certainty. A simulation study involving a small number of Christchurch houses was conducted to replicate typical exposures during removal work (in terms of duration and dustiness) that was carried out in the first year after the earthquakes, before stricter procedures for asbestos monitoring and abatement were fully operational. The resulting exposures were found to be well below the permissible workplace exposure standard even for full-time abatement work over a 3-year period, and it was therefore concluded the risk to occupants (who would have experienced only short duration exposures during this time) would have been extremely low. Is the public at risk? Assessment of the current scientific knowledge on exposure levels and risks associated with home remediation activities such as those that have taken place (and are still in progress) in Canterbury indicates that they are unlikely to result in a significant increase in risk to homeowners and occupants of damaged houses, unless they were performing the work themselves, without taking proper precautions such as wetting the surfaces and using a respirator. A simulation study showed that even in a scenario of uncontrolled removal of potentially friable ACMs by dry scraping methods, asbestos concentrations in air in the vicinity of workers respirators did not reach regulatory levels. It is nonetheless very important that correct procedures for dealing with asbestos during remediation work are followed, and homeowners undertaking repair and renovation work themselves should be made aware of the potential hazard if asbestos is disturbed. Overall, the risk is considered to be low if proper precautions are taken, but it is recommended that repair or removal of friable ACMs are handled by professionals who are trained in the correct procedures. Neither alarm nor complacency about the level of risk to bystanders is warranted. While there has also been concern expressed about the dust present in the air in the immediate aftermath of the earthquake, data from major earthquakes elsewhere are reassuring. 4

11 Review methodology This report set out to evaluate the peer-reviewed scientific literature on the health risks associated with asbestos exposure at the levels that may be encountered in the home environment in New Zealand, with specific reference to exposure type and duration in situations such as home renovation and/or repair, or during earthquake recovery. Literature searches were undertaken (with no date limit) in Medline, EMBASE, the Cochrane library database, Scopus, and Web of Science in order to identify relevant studies relating to low-level, nonoccupational asbestos exposure in the peer-reviewed scientific literature. The particular focus was on asbestos exposures to occupants of homes containing ACMs, and effects of renovation, repair, or removal of ACMs on airborne asbestos fibre levels. Very few studies were identified; therefore studies detailing occupational exposure levels and associated risks of asbestos-related diseases were used as a base for comparison and extrapolation to low-level exposure. The review did not include studies relating to asbestos exposures (either occupational or nonoccupational) from machinery insulation or friction products such as motor vehicle brake linings, although such products still exist in New Zealand and may contribute to occupational exposures in the mechanical trades, and environmental exposures to the public. Reports and commissioned studies from recognized national and international bodies (NZ Ministry of Health, WorkSafe NZ, World Health Organization, International Agency for Research on Cancer, US Environmental Protection Agency, US Public Health Service, UK Health and Safety Authority, Safe Work Australia) were considered where relevant. 5

12 Asbestos exposure in New Zealand: Review of the scientific evidence of nonoccupational risks 1. Asbestos background 1.1 Types and characteristics Asbestos is a general term encompassing a number of naturally occurring fibrous silicate minerals found in certain types of rock formations that are abundant around the globe. [1] The discovery of the many useful properties of asbestos, including high tensile strength, resistance to fire, very low thermal conductivity, and resistance to acid corrosion, led to its use as an insulating, fireproofing, and strengthening material in a vast number of industrial applications. [2] The asbestiform habit refers to mineral crystals that grow in a single dimension, as opposed to random, multidimentional prismatic patterns. Asbestiform minerals form long, threadlike fibres that bend like wire rather than shattering under pressure. There are two families of asbestos types; the serpentine family is characterized by curly fibres, and comprises a single member known as chrysotile asbestos. The amphibole group, characterized by long, straight, and thin fibres, consists of amosite, crocidolite, tremolite, anthophyllite and actinolite fibre types. The types of asbestos that were most commonly used in building products are chrysotile, amosite, and crocidolite, whereas tremolite, anthophyllite and actinolite are noncommercial contaminants. While the amphiboles share certain crystal features, all asbestos types differ in their chemical composition (see Table 1 and Figure 1). [3] The varying characteristics of the different asbestos types influence their effects on the human body (see section 3.1). Table 1. Asbestos types and characteristics Fibre type Typical formula* Description Chrysotile Mg 3Si 2O 5(OH) 4 Serpentine. White colour. Curly fibres, faster lung clearance. Fibres undergo longitudinal splitting Amosite (Fe 2+ Mg) 7Si 8O 22(OH) 2 Amphibole. Brown colour. Crocidolite (Na 2Fe 3 2+ Fe 2 3+ )Si 8O 22(OH) 2 Amphibole. Blue colour. Tremolite Ca 2Mg 5 Si 8O 22(OH) 2 Amphibole. Anthophyllite (Mg, Fe 2+ ) 7 Si 8O 22(OH) 2 Amphibole. Brown colour. Actinolite Ca 2(Mg, Fe 2+ ) 5Si 8O 22(OH) 2 Amphibole. * there is variability in composition because the silicate framework can accommodate a mixture of many different ions 6

13 Figure 1. Asbestos types/families Serpentine family Chrysotile Asbestos Amphibole family Commercial types Crocidollite Amosite Actinolite Non-commercial, contaminating types Tremolite Anthophyllite. 1.2 Historical use and hazard recognition Inherent to virtually all innovations throughout history is the fact that while they are developed for a human benefit, they also carry potential risks of harm. [4] The industrial utilization of asbestos as a fireproofing material is a prime example of a technological advance that was developed to reduce a known risk catastrophic fire - but was later found to carry considerable risks of its own. [5] Once referred to as the miracle mineral, asbestos is now known to be a human carcinogen, and therefore a public health hazard. Inhalation of its airborne fibres can cause pleural changes, asbestosis, lung cancer, and mesothelioma, depending on the intensity and duration of exposure. Asbestos exposure has also been associated with increased risk of laryngeal and ovarian cancers following heavy exposure. Asbestos came into widespread use in the early 1900s, when fire risk featured prominently in the public consciousness. With the advent of new technologies using steam, kerosene and electricity, new fire hazards were emerging and fire was a constant threat. Experiences with catastrophic fires, involving hundreds of casualties in public buildings (theatres, schools, office buildings) and on ships, motivated the search for a building and insulating material that was non-combustible and had low thermal conductivity. Asbestos, long known for its strength and resistance to fire and chemical breakdown, seemed ideal. [6] It was mined extensively in several countries (Canada, South Africa, Australia, Russia, China, Brazil, Zimbabwe, Kazakhstan, and India) and came to have significant industrial and economic importance throughout the world. Russia is currently the largest producer of asbestos, followed by China, Brazil, and Kazakhstan. Canada, formerly one of the world s top asbestos producers and exporters, halted mining operations in Reports of serious respiratory problems began to emerge in the early 20 th century in asbestos miners and workers handling raw asbestos in the manufacture of asbestos products (textiles, insulation, building materials etc.). The first disease to be associated with asbestos exposure in the workplace 7

14 was termed asbestosis, a progressive scarring disorder (fibrosis) of the lungs. By the 1960s, a significant excess of asbestosis, as well as lung cancer and malignant pleural mesothelioma, had emerged in workers involved in installing and maintaining asbestos products, including plumbers, electricians, mechanics, ship builders and construction workers. [7] More recently, the consequences of asbestos exposure have been noted in people engaged in repair, renovation, and removal of ACMs. [8, 9] The use of crocidolite asbestos, and the spraying of any type of asbestos, has been prohibited since 1986 under the International Labour Organization Convention No. 162, [10] but chrysotile asbestos continues to be used in asbestos cement products in a number of low- and middle-income countries. People all over the world are still being exposed to asbestos, not only in those countries where its use is still common, but also in those that have banned its use but still have vast quantities of ACMs present in public buildings and homes. 1.3 Hazard, exposure, vulnerability and risk It is important to distinguish between hazards and risks and to understand the impact of exposure and vulnerability, because these concepts are critical for informed decision-making and risk communication. [4] A hazard is something with an intrinsic propensity to cause harm, whereas a risk is the likelihood that exposure to a hazard will result in harm. This likelihood is dependent on the vulnerability of the population, and their extent of exposure to the hazard. We can avoid the risks of hazards by reducing our exposure to them. A hazard with no exposure poses no risk. The very high levels of exposure to asbestos that occurred in occupational settings before its hazardous properties were well known have cost many workers their lives, and others are still at risk of developing disease due to past heavy exposures. There is evidence that lower exposures, such as those that occur from encountering airborne asbestos fibres while living in the vicinity of asbestos mines and factories, and even brief but intense or intermittent non-occupational exposure can also increase the risk of asbestos diseases, in particular mesothelioma. No safe lower limit of exposure has been identified with certainty all exposures are thought to add to the overall risk of disease development but the risk from a single, low-level exposure is considered to be extremely low. Awareness of the potential for exposure is nonetheless very important if risks are to be minimized. Although work-related exposures have decreased, diseases resulting from exposure to deteriorating ACMs in older houses represent a potential public health issue for the future. There are reports of schoolteachers who have contracted mesothelioma for whom the likely contact was from friable inplace ACMs in schools [11, 12] Custodians and maintenance workers in public buildings have also developed asbestos-related diseases. [11] The problem of unrecognized asbestos exposure is an important health issue in settings where it is not controlled or not appreciated. The risk to the general public depends not only on the effect of cumulative low-dose exposures, but also the relative vulnerability (susceptibility) of individuals to disease development. One factor influencing disease susceptibility is cigarette smoking, which greatly amplifies the risk of lung cancer associated with asbestos exposure beyond the combined effects of the individual risk factors. This means that smokers are much more susceptible to asbestos-induced lung cancer than are nonsmokers. Smoking does not have an impact on the risk of mesothelioma or other asbestos-related cancers. There is some evidence of genetic susceptibility to mesothelioma; for example, BAP1 gene mutations greatly increase mesothelioma risk in asbestos-exposed individuals. [13] This may partially explain why some individuals develop mesothelioma following low-level asbestos exposure, while 8

15 others with high-level exposure do not. [14] Very little is known about what other factors may influence susceptibility to these diseases, but it is clear that individuals exposed to the same asbestos hazard do not all respond in the same manner in terms of disease development. The generally low exposures experienced today do not pose an increased risk for fibrotic lung disease (asbestosis), which requires very high-dose fibre inhalation to trigger its development. [15, 16] Levels of asbestos exposure in most contemporary environments are also not expected to result in a quantifiable increase in risk of lung cancer above the background incidence, though the risk should not be considered zero, particularly among smokers. The potential risk of developing mesothelioma, which is very strongly associated with asbestos exposure and has an otherwise low background incidence, remains an issue. Therefore this report will focus on the risks to the public of developing mesothelioma from exposure to asbestos in the non-occupational environment in New Zealand. 2. Asbestos-related diseases All types of asbestos are known to cause fibrotic lung disease (asbestosis), pleural plaques, diffuse pleural thickening and pleural effusions, lung cancer, malignant pleural mesothelioma, laryngeal cancer and possibly other cancers with varying latency periods. The International Agency for Research on Cancer (IARC) has also accepted that there is sufficient evidence to indicate that women with a history of heavy occupational or environmental exposure to asbestos are at an increased risk of developing ovarian cancer. [17] The consequences of exposure are generally seen only many years after the exposure began, and often long after it has ended. The earliest IARC report on asbestos in 1973 stated that all major commercial forms of asbestos can produce malignant mesotheliomas in animals, and that heavily exposed workers were at significantly increased risk of lung cancer and mesothelioma. [17] Asbestos has been listed in the US as a known human carcinogen since the first National Toxicology Program (NTP) report on carcinogens in 1980, [18] and is recognized by the WHO as one of the most important carcinogens worldwide, with a burden of disease that continues to rise despite declining industrial asbestos use. [8, 19, 20] The epidemiological evidence has only strengthened over time and there is currently overwhelming evidence that all commercial forms of asbestos fibres are causally associated with an increased risk of mesothelioma and lung cancer, despite ongoing uncertainty over the extent to which the various forms differ in potency. [21] Most asbestos-related diseases are clearly dose related their development depends on the intensity and duration of exposure. There remains some scientific uncertainty regarding the varying toxicities of chrysotile versus amphibole asbestos, as well as the risk of minimal exposure. To date no safe level has been convincingly demonstrated, but such a demonstration would be very difficult given that some very low level of exposure to asbestos is experienced by everyone. The major health concerns arising from asbestos exposure are detailed below. 9

16 2.1 Benign pleural disease Benign pleural changes including diffuse pleural thickening, pleural effusion (fluid around the lungs), and pleural plaques are commonly observed in asbestos-exposed workers. Such changes are often asymptomatic, but can sometimes result in abnormal lung function or pain. Pleural plaques, which appear as discrete areas of thickening on the parietal pleura, are the most common manifestation of asbestos exposure. The incidence increases with increasing exposure duration, but may also occur after relatively low-dose exposures. Benign asbestos effusions are an early manifestation of asbestos disease, sometimes occurring within 10 years of exposure, but usually resolve within a few months. [22] These types of changes do not have any implications for the likelihood of developing an asbestos-related cancer, except by indicating that there has been exposure to asbestos. 2.2 Asbestosis The most serious non-malignant asbestos-related disease is asbestosis. Asbestosis was first reported in the early 20 th century as diffuse fibrosis leading to scarring of the lungs, resulting from inhalation of very high doses of asbestos fibres. Fibrosis progresses after cessation of asbestos exposure. As the disease progresses, the lungs contract progressively until they may no longer be able to expand with each breath sufficiently to support respiration. A high fibre concentration in the lungs is required for development of asbestosis, which was once frequent among heavily exposed worker populations. In fact, patients with asbestosis always have a history of high occupational asbestos exposure. [23] As a result of more stringent control of such exposures in the workplace, as well as the decreasing industrial use of asbestos, the incidence of this disease is now declining. It has never been reported as a consequence of casual or environmental exposure, and is not known to be an issue with current exposure levels either occupationally or involving the general public. [16] 2.3 Lung cancer An increased incidence of lung cancer in asbestos workers was first suspected in the 1930s, but the linking of asbestos with excess occurrence of lung cancer was not fully appreciated until the 1950s, following publications by Doll [24] and Breslow [25] among others. Asbestos-related lung cancers are clinically indistinguishable from those due to other causes such as cigarette smoking. In the mid- 1960s, Selikoff and colleagues reported an added effect of tobacco smoking on the risk of lung cancer in asbestos insulation workers. [26] The effects of smoking and asbestos exposure on lung cancer risk are synergistic, meaning that the combined risk for the development of lung cancer is significantly higher than the sum of the individual risks. Like asbestosis, lung cancer has mainly been observed in people with high occupational exposure to asbestos, rather than as a result of low-level environmental exposure. [21] Nonetheless, the risk should not be considered to be completely absent in the non-occupational environment, particularly among tobacco smokers, in whom the lung cancer risk is markedly amplified above that of non-smokers for the same level of asbestos exposure. 2.4 Mesothelioma Mesothelioma is an uncommon, aggressive cancer of the mesothelium, which lines the pleural, pericardial, and abdominal cavities and the outer surface of the lungs, heart, and abdominal organs. The strong link between asbestos exposure and development of malignant pleural mesothelioma 10

17 was first made by Wagner in 1960 [27] and supported by the work of Selikoff. [28] In 1986 the US Environmental Protection Agency (US EPA) concluded that the risk of death from mesothelioma was directly related to the length of time since the start of a person s occupational exposure to asbestos. [29] The increasing incidence of mesothelioma since the mid-1970s follows the earlier trend of increasing widespread use of asbestos. The etiological link between asbestos and mesothelioma is now well documented, such that mesothelioma is considered a clinical sign indicating asbestos exposure, although there is a very low background rate independent of known asbestos exposure. The crude background incidence rate for mesothelioma is estimated at 1-2 per million people per year. [30] Over the period , a total of 95,253 mesothelioma deaths were reported to WHO from 83 countries, equating to an age-adjusted death rate of 4.9 per million per year. The mortality rate more than doubled during the 15-year study period, probably reflecting both better disease detection and a real increase in incidence. The mean age at death was 70 years. [30] A high incidence of mesothelioma was observed in men born around throughout Western Europe, reflecting the extent of asbestos use in the 1960s and 1970s when this cohort was entering the workforce. [31] Mesothelioma does not just affect workers in the asbestos industry; it has affected brake mechanics (chrysotile was commonly used in brakes until mid-1980s in US), [32] railway workers, and construction trades. [33, 34] Many high-risk occupational exposures and activities have now ceased. A large proportion of people currently dying of mesothelioma have previously worked in building construction and maintenance, and this sector now constitutes the largest occupational risk group (see section 5 on exposures/risk assessment). Most cases of mesothelioma are associated with asbestos exposure, but some are not. [35] The only other recognised risk factor for pleural mesothelioma is exposure to erionite, a naturally-occurring fibrous silicate mineral with similar structure to amphibole asbestos but different chemical and physical properties [36] Erionite is present in some volcanic ash deposits in New Zealand, Germany, Russia, Japan, Kenya, Turkey, Italy, and in the western United States. A very high incidence of mesothelioma was observed in the 1970s in several villages in Turkey, where erionite was present in zeolite stones used to build houses. The annual incidence was 800 cases/100,000 population, which is 1000 times the rate observed in the general population of industrialised countries. [37] The potency of erionite as a human carcinogen appears to be higher than that of asbestos, particularly for the development of mesothelioma. While there is evidence that a true background incidence of mesothelioma exists, [33] underreporting of asbestos exposure and/or possible misdiagnosis of malignant mesothelioma (because the diagnosis can be difficult to establish) may account for some presumed non-asbestos related disease. [38] Because mesothelioma has been noted in individuals with relatively low exposure to asbestos, the incidence of this disease is considered the most sensitive indicator of asbestos exposure in a population. 2.5 Other cancers Epidemiological studies have shown associations between asbestos exposure and cancers of the oropharynx, larynx, oesophagus, stomach, colon, rectum and ovary [39] In each case the evidence is less substantial than for asbestosis, lung cancer, and malignant mesothelioma. An IARC Working Group in 2012 concluded that a causal association is clearly established for cancers of the larynx and ovary [21]. Since inhaled asbestos fibres pass through the larynx, they may become deposited there. Asbestos fibres have been found in the ovaries of women who were exposed to asbestos either in an 11

18 occupational setting, or from residing in a contaminated asbestos mining area or living with an asbestos worker. However, the route by which asbestos fibres reach ovarian tissue has not been clearly established. [40] Causal associations between asbestos exposure and risks of other cancers have not been confirmed. 3. Mechanisms of asbestos toxicity Asbestos fibres cause damage when inhaled into the lungs, where they can penetrate deep lung tissue and remain deposited for many years, exerting fibrotic, inflammatory and mutagenic/carcinogenic effects. These effects are modified by factors that determine the respirability (potential for inhalation into the small distal airways), bioactivity, and clearance of fibres from the lungs. 3.1 Determinants of toxicity While all types of asbestos share the same hazards, i.e. the potential for lung cancer, asbestosis and mesothelioma, they have varying degrees of risk - the likelihood that disease or death from the hazard will occur. The physical and chemical makeup of fibres, including crystallinity, surface reactivity, and the presence of transition metals, determines fibre stability in the body and the biological response to the contaminant, and therefore influences the carcinogenic potential of a particular fibre type. [19] Crocidolite is an iron-rich asbestos fibre that is considered the most pathogenic for causing mesothelioma. [41] Critical determinants of asbestos toxicity are fibre dimensions, dose and durability. Dimensions For measurement purposes, asbestos fibres are defined as having a minimum length of 5µm and an aspect ratio (length to diameter) of 3:1. The most important property of asbestos for respirability is fibre diameter. Smaller diameter fibres (<0.5 µm) exhibit greater penetration to distal portions of the lung, because they can align longitudinally in small airway passages and reach the alveoli. Respirability and deposition are also determined by fibre length - although shorter fibres are respirable, they can be engulfed by macrophages and removed, whereas longer fibres cannot. [19] Animal studies demonstrate that long, thin fibres are more pathogenic than short, coarse/thick ones, [42] though fibres of all lengths have the potential for toxicity. [43] Chrysotile fibres have physical characteristics that are unique among the asbestos types, and that greatly influence its aerodynamic properties and respirability. Whereas amphiboles exist as single fibres in air, chrysotile fibres tend to clump together, meaning they are less readily transportable to the deep lung airways compared with amphibole fibres. Dose The intensity and/or duration of exposure influences the capacity of macrophages in the lungs to engulf and remove fibres. Short but intense exposures can overwhelm the lungs capacity for clearance, allowing more fibres to become deposited. However, even with low dose exposure, asbestos fibres can accumulate in the lungs over time, so the duration of exposure is an important factor in assessing the asbestos fibre lung burden. 12

19 Both cohort and case-control studies have demonstrated a dose-response relationship between asbestos exposure and risk of mesothelioma. There is no evidence of a threshold for the carcinogenic effect of either amphibole or chrysotile types of asbestos; in theory even very low doses could trigger pathogenic reactions in the lungs, eventually leading to cancer, but the risks increase substantially with increasing dose intensity and duration of exposure. It appears that mesothelioma can be triggered by lower exposures than those that lead to lung cancer or other cancers. In contrast, very high intensity exposures are required to trigger asbestosis. [16] Durability/biopersistence Fibre durability relates to how fast a fibre will dissolve in body fluids, and other factors that affect its persistence in body tissues. Most asbestos fibres do not dissolve readily in lung fluid. Chrysotile is the most soluble of the asbestos types because of its chemical composition: the magnesium hydroxide content of chrysotile is removed in solution in a time-, temperature- and ph-dependent manner, leaving an insoluble silica skeleton. The amphibole contaminant tremolite is the least soluble of asbestos types, and has been considered one of the most hazardous. The solubility of asbestos types decreases from chrysotile (most soluble) to tremolite (least soluble) as follows: chrysotile > amosite > actinolite > crocidolite > anthophyllite > tremolite [19, 44] Once inhaled, all varieties of asbestos fibres become deposited throughout the respiratory tract, but often accumulate at bifurcations of larger airways, where lung cancers tend to initiate. Over time after exposure, the average length of retained fibres increases, and diameter decreases, meaning that longer, thinner fibres are cleared more slowly than shorter, thicker ones. [8] The straight, needlelike fibres of amosite and crocidolite asbestos can split longitudinally, becoming thinner, but otherwise are resistant to degradation and can remain in the body for 40 or more years. The very fine fibres can migrate through lung tissue into the pleura. In contrast, curly chryostile fibres tend to degrade chemically, therefore showing shorter residence time in the lung. These factors affect the biopersistence of fibre types, and have implications for their toxicity. 3.2 Biological mechanisms While asbestos has long been classified as carcinogenic, [45] the exact mechanisms through which asbestos fibres exert their carcinogenic and other effects have not been fully elucidated. Some identified mechanisms include macrophage activation, inflammation, generation of reactive oxygen and nitrogen species (ROS and RNS), tissue injury, genotoxicity, changes in chromosome number, and altered gene expression affecting cell survival and proliferation. [21] Carcinogenesis is a multistage process. Both direct and indirect fibre genotoxicity can cause mutations that allow the initial escape of cells from normal growth control and promotion and progression of tumour growth. Over time, a series of oncogenic events occurs that leads progressively towards more invasive cancer. The known synergism between asbestos and tobacco smoke for the development of lung cancer but not for mesothelioma suggests that the mechanism for carcinogenicity of asbestos fibres may differ in different target cells. [46] 13

20 4. Asbestos use in New Zealand Asbestos importation to New Zealand began in the late 1930s and peaked in 1974, when the annual amount imported totaled more than 12,000 tons. Imports declined rapidly after this time. There was some limited mining of raw chrysotile asbestos near Takaka in the 1950s, but it was of poor quality and had to be mixed with imported asbestos. ACMs came into New Zealand before World War II as wall claddings, pipes, and cements. In 1938 and 1943 two ACM manufacturing plants were established in New Zealand (in Auckland and Christchurch). These industries mainly manufactured asbestos-cement building products containing around 5 to 15% asbestos. [47] From around 1960, the predominant asbestos type used in buildings in New Zealand and most other industrialized countries was chrysotile. Smaller amounts of crocidolite and amosite were used in building products prior to [48] In addition to its construction uses, asbestos was used in New Zealand for machinery insulation, insulating tapes and cloths, gaskets and seals (particularly in the aviation and marine industries), and friction materials (e.g. brake linings) for motor vehicles. [49] This report will focus on exposures from products that were used in the construction of residential houses in New Zealand. In terms of kilograms of asbestos used per capita per year, asbestos use in New Zealand was lower than in many industrialized countries until the 1970s-1980s, when per capita use exceeded that of the USA and the UK, though it remained substantially lower than in Australia, Canada, Germany, and Denmark. [21] The cumulative amount of asbestos imported into New Zealand over time totals more than 200,000 tons, much of which is still in place in buildings, homes, and machinery insulation. [47] Despite the known health risks, and in contrast to many Western industrialized countries, the use of materials containing chrysotile asbestos is not yet banned in New Zealand, and import of such material is not strictly regulated. The importation of raw crocidolite and amosite asbestos was prohibited by a succession of temporary Customs Import Prohibition Orders (CIPO) beginning in 1984 for amosite and crocidolite and in 1999 for chrysotile. [49] The most recent CIPO expired in 2008, when it was effectively replaced by the Hazardous Substances and New Organisms (HSNO) Act 1996 approval process. All forms of asbestos are regarded as unapproved hazardous substances under HSNO, but are not strictly banned. Theoretically, approval could be sought from the New Zealand Environmental Protection Authority (NZ EPA) to import asbestos into New Zealand, if it could be shown that the benefits outweigh the risks and costs to the environment and public health, but such approval would be very unlikely. Nonetheless, it is possible that some ACMs containing chrysotile asbestos are still entering the country. [50] A recent inventory of product imports noted significant uncertainties and discrepancies in the data and suggested that there may be cases of imported products being incorrectly labeled as containing asbestos, and also of asbestos-containing products that have been declared as asbestos-free. [49] However, a survey that included building industry groups (NZ Building Industry Federation [BIFNZ], Claddings Institute of NZ, NZ Fibrous Plaster Association, Building Research Association of New Zealand [BRANZ]), found that there are very few current uses of ACMs, and in almost all cases (aside from replacement parts for some aircraft), substitutes for asbestos have been in use for a long time. The survey found no evidence or knowledge of imported products containing asbestos, or of any companies supplying ACMs. [49] This is, however, no guarantee that products imported from countries still manufacturing ACMs are asbestos free, whether or not they are labeled as such. Even where bans are in place, imports can slip through. For example, wall tiles imported into Australia from China in 2010 were found to contain tremolite asbestos despite this being a banned substance. [51] 14

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